POS0673 ENDOTHELIAL INFLAMMATION IN RHEUMATOID ARTHRITIS PATIENTS TREATED WITH TOFACITINIB
Authors: M. DeLaVega, C. Peon, G. Rodriguez, F. Benavidez, A. Benitez, M. J. Gamba, M. Eleta, A. Riopedre
Journal: Annals of the Rheumatic Diseases (2022)

Background Systemic inflammation in rheumatoid arthritis (RA) seems to accelerate atherosclerosis process and increased cardiovascular (CV) events. An adequate joint inflammation control is correlated with endothelial inflammation (EI) improvement. 18F-fluorodeoxyglucose positron emission tomography with computed tomography (FDG PET/CT) has been shown as a non-invasive, sensitive, and specific tool to show EI. Maximum standardized uptake value (SUV(max)) greater than 1,6 has been correlated with vascular and joint inflammation. Tofacitinib is a Jak inhibitor (JaKi) approved for RA that improves activity and function. The aim of this study is to evaluate the EI outcome by FDG-PET in RA patients treated with tofacitinib. Objectives To assess the EI by FDG-PET/CT in RA patients at baseline and after 12 weeks of tofacitinib treatment initiation. To correlate the vascular findings with disease activity, lipid profile and carotid atherosclerosis by echo Doppler. Methods Prospective, observational study. Inclusion criteria: RA (ACR 2010) patients &gt;18 years old, with high activity score (DAS 28 &gt;3,2) and with biologics or synthetic Dmards requirement by Treat to Target strategy and who tofacitinib was prescribed. Exclusion Criteria: Biologics or Jaki previous use or major CV history known. A baseline Visit evaluating disease activity (DAS 28 and CDAI), functional status by Health Assessment Questionary (HAQ), CV and smoking history, treatments and lipid lab assessment was performed. EI was measured by PET-FDG/CT, showing the SUVmax and target-to-background ratio (TBR) in: right primitive carotid, left primitive carotid, ascendent aorta, descendent aorta and abdominal aorta. Carotid echo Doppler for showing plaque presence was done. During baseline visit tofacitinib was started. After 12 weeks the initial parameters were re-evaluated. Results Consecutively, 30 patients were included. Mean age 57 yo (21-79). Female 70%. Mean disease duration 8,3 years (1-40), mean Body mass index (BMI) 24,5. Clinical history: Hypertension 27%, smoking 6,6%, methotrexate treatment 46,6%, methotrexate plus leflunomide 50%, corticosteroids 7,6% (mean dosis 7,6 mg/day). Mean values of DAS 28, CDAI and HAQ were 5.21, 26,6 y 1,56 in baseline and 3,04, 8,80 y 1,09 in the final visit respectively (p:&lt; 0,001 in all comparations) showing statistical significance activity improvement. Echo doppler showed Carotid plaque in 40% of patients without change between visits. Mean cholesterol levels were 188,5 y 207,53 mg/dl in baseline and final visit respectively (p: 0,0039), showing statistical significance. Endothelial uptake by PET-FDG in the 5 areas measured, considering baseline and final visit was: Right Primitive Carotid: SUV Max 2,03 and 1,93 (p: 0,32) and TRB Max 0,94 and 0,85 (p:1,0); Left Primitive Carotid Suv Max 2,07 and 1,94 (p:1,0) and TRB Max 0,92 and 0,90 (p:0,57); Ascendent Aorta SUV Max 2,63 and 2,57 (p:1,0) and TRB Max 1,18 and 1,15 (p:1,0); Descendent Aorta SUV Max 2,77 and 2,57 (p:0,26) and TRB Max 1,27 and 1,17 (p:0,26) and Abdominal Aorta SUV Max 2,59 and 2,43 (p:0,85) and TRB Max 1,15 y 1,11 (p:0,32). None of the endothelial uptake comparisons showed a significant difference between baseline and final visit after 12 weeks. Conclusion This work shows that, despite the significant improvement in joint activity and function values, there was no modification in EI measured by FDG-PET during tofacitinib treatment along 12 weeks. It is noteworthy that all patients initially presented high inflammatory endothelial uptake values, which reinforces the hypothesis of vascular compromise associated with active joint disease. Studies with more observation time and evaluating the role of different treatments related to endothelium will be of clinical utility in the future. References [1]Rheumatology (Oxford). 2016 Oct;55(10):1777-85. [2]Metabolism. 2017 Feb;67:72-79. [3]Arthritis Res Ther. 2016 May 21;18(1):115. Acknowledgements Pfizer´s unrestricted grant Disclosure of Interests None declared